Myelin-derived ephrinB3 restricts axonal regeneration and recovery after adult CNS injury

The study investigates the role of ephrinB3, a protein found in myelin, in limiting axon regeneration after central nervous system (CNS) injuries. The research uses mice lacking a functional ephrinB3 gene to examine axon regeneration following optic nerve crush and spinal cord injury. The experiments showed that without ephrinB3, there was a significant increase in axon regeneration after both optic nerve and spinal cord injuries. This suggests that ephrinB3 contributes to the failure of axons to regrow after CNS trauma. The findings indicate that targeting ephrinB3 could be a therapeutic strategy to promote axon regeneration and improve recovery after CNS injuries. However, the study also notes complexities, such as altered gait and spasms in ephrinB3-deficient mice, indicating a need for careful consideration in therapeutic development.

• 1
  EphrinB3 contributes significantly to the inhibitory activity of myelin, restricting neurite outgrowth of dorsal root ganglion cells in vitro.
• 2
  Mice lacking ephrinB3 show significantly increased axonal regeneration after optic nerve crush injury, demonstrating a role for ephrinB3 in limiting optic nerve regeneration in vivo.
• 3
  After spinal cord injury, ephrinB3−/− mice exhibit improved locomotor performance and increased corticospinal and raphespinal growth in the caudal spinal cord after a dorsal hemisection injury.